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The overnight reduction of amyloid β 1‐42 plasma levels is diminished by the extent of sleep fragmentation, sAPP‐β, and APOE ε4 in psychiatrists on call
Author(s) -
Grimmer Timo,
Laub Theresa,
Hapfelmeier Alexander,
Eisele Tamara,
Fatke Bastian,
Hölzle Patricia,
Lüscher Sandra,
Parchmann AnnaMareike,
Rentrop Michael,
Schwerthöffer Dirk,
MüllerSarnowski Felix,
Ortner Marion,
Goldhardt Oliver,
Kurz Alexander,
Förstl Hans,
Alexopoulos Panagiotis
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.12072
Subject(s) - sleep deprivation , fragmentation (computing) , medicine , apolipoprotein e , endocrinology , amyloid (mycology) , sleep (system call) , disease , psychology , circadian rhythm , biology , pathology , ecology , computer science , operating system
In mice there might be an association between sleep deprivation and amyloid β plasma levels. Hence, we examined whether amyloid plasma levels are associated with sleep duration or fragmentation in 17 psychiatrists on‐call. Methods Amyloid β (Aβ)42, Aβ40, and soluble amyloid precursor protein β (sAPP‐β) plasma concentrations were measured at the beginning and end of 90 on‐call nights, and analyzed using generalized linear models. Results In on‐call nights, a 10.7% reduction of Aβ42 was revealed overnight. Every single short sleep interruption diminished this reduction by 5.4%, as well as every pg/mL of sAPP‐β by 1.2%, each copy of APOE ε4 by 10.6%, and each year of professional experience by 3.0%. Discussion The extent of sleep fragmentation diminishes the physiological overnight reduction of Aβ42 but not Aβ40 plasma levels in the same direction as the enzyme for Aβ42 production, the genetic risk factor for Alzheimer's disease (AD), and on‐call experience. Might on‐call duty and sleep fragmentation in general alter the risk for AD?